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Category Archives: Haematology

CKD and Anaemia

Chronic kidney disease is frequently connected with anaemia; eGFR is used to indicate the degree of kidney function, and determine which of five stages the patient falls into. Anaemia is associated with decreased renal function as the production of erythropoietin (EPO) declines in accordance with low Hb levels. Patient may present with symptoms of tachycardia, fatigue, reduced cognitive function or left ventricular hypertrophy.

Combined with CKD, anaemia can exacerbate other conditions such as diabetes and cardiovascular disease. Human EPO may be prescribed, although it can have the side effect of exacerbating hypertension.

As in all other cases, the cause for the anaemia should be sought in order that the most appropriate treatment can be commenced. The cause may be renal, or it may be caused by iron, folate or b12 eficiency, hypothyroidism, hyperparathyroidism, bone marrow infiltration, chronic inflammation or infection, chronic haemorrhage, aluminium toxicity, pure red cell aplasia, haemolysis or malignancy.

Low Hb can indicate anaemia, it is therefore important to check FBC routinely to review WCC and platelet count to rule out infection and find haematological causes of anaemia. Low white cell and platelet counts can indicate involvement of the bone marrow, whereas if WCC and platelet count is high, this could be associated with inflammation or infection. Acceptable platelet range is 150-400 x 109/l

Parathyroid hormone (PTH) controls calcium levels, ensuring that vitamin D and calcium are absorbed, preventing bone damage. PTH should be measured in all CKD patients with an eGFR <60ml/min/1.73m2. PTH of less than 100pg/ml can show bone disease.  It is important to measure PTH as way of identifying bone condition, as hyperparathyroidsim is associated with bone marrow fibrosis. Hyperparathyroidism can also reduce the response to ESA therapy. However, there is no need to measure TSH at this time.

Serum ferritin should be maintained at 200-500micrograms/l. Haemodialysis patients should be prescribed iron supplements to achieve and maintain this level.

Efficacy of ESA therapy can be reduced by inadequate dialysis. Adequacy of dialysis can be measured by urea reduction ratio before and after dialysis, and for haemodialysis patients levels should be above 65%.

Reticulocytosis can be caused by haemolysis, acute or chronic blood loss. A FOB test maybe required to check for GI bleeding. Anaemia can also be caused by GI tract cancer, so colonoscopy can be performed to exclude cancer.

A positive haemolysis test may indicate anaemia caused by a na infection, or reaction to a drug/infusion, or an autoimmune disorder such as SLE. Bilirubin is raised in patients with a higher level of haemoglobin.

C-reactive protein levels should also be checked as CRP is a marker for inflammation. Ferritin levels can be affected by inflammation, and so determining if there has been inflammation (with the CRP) can aid diagnosis. CRP will help to show whether the anaemia is caused by inflammation or infection. If CRP is normal, the ferritin level can be trusted.

Generally there are two causes for iron deficiency, if it is not due to haemorrhage, it may be due to haemolysis.

Serum creatinine is affected by GFR as well as age, gender, weight, diet, medication, race, and also some laboratory methods. This is a poor test to determine renal function in the elderly. Drugs that affect GFR include ACE inhibitors in patients with renal vascular disease, as will diuretics. It is therefore good practice to check GFR before initiating treatment with these drugs, as well as two weeks after beginning treatment, checking regularly after this as routine. If there is big decrease in GFR, other causes must be ruled out, if ACEI is causing the reduction in GFR, it may need to be discontinued. ACEIs can also affect haemoglobin levels even if previously stable.

ESA treatment should only be considered if Hb levels are not increased with ferritin

 
 

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Thrombophilia

Thrombophilia, as the name implies is a blood disorder that increases the risk of clotting and therefore increases the risk of venous thromboembolism. It can be acquired through conditions such as heart failure, irritable bowel syndrome and nephritic syndrome. Or it may be inherited. Up to half of those treated for VTE are thought to have hereditary thrombophilia. This is known because patients who have had VTE are routines screened to see if there was an inherited factor in their episode. If a family member has had a previous VTE, genetic screening can be offered to identify and deal with the risk in others. Tests are carried out a month after anticoagulant treatment has finished as these interact with the antithrombin, protein S and protein C that are screened for deficiencies.

The risk of developing VTE in patients with thrombophilia is increased with dehydration and immobility/inactivity, surgery (particularly major general surgery and orthopaedic surgery to the legs) leg fractures, hip fractures, spinal cord inury, varicose veins or congestive heart or respiratory failure. Some forms of contraception can also increase the risk of VTE, therefore they are not normally recommended for patients with hereditary thrombophilia. The progestogen only pill (POP) is generally used instead of combined oral contraceptives. Pregnancy is also a risk factor, particularly if the mother is obese or more mature. This is the biggest cause of maternal mortality, especially after Caesarean section. Cancer patients are at increased risk too, but there’s also a secondary risk with chemotherapy.

In the acute setting, patients will generally be prescribed five days of anti-coagulation treatment with low molecular weight heparin (LMWH) or unfractionated heparin (if in renal failure). This is then followed by six months of oral anticoagulants. Because of the increased risk of haemorrhage, anticoagulants are not normally continued in such cases after six months.

 
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Posted by on March 6, 2012 in Haematology

 

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Anaemia and Non-Inflammatory Respiratory Disease

According to the International Journal of Clinical Practice (2001. 65:479-486) around 10% of patients with severe non-inflammatory respiratory diseases suffer from anaemia. It is already known that there is a link between COPD and anaemia.

 
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Posted by on February 27, 2012 in Haematology, Respiratory

 

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